Acute coronary syndrome

Question 1

What is ACS?

Answer 1

Acute coronary syndrome (ACS) is an umbrella term covering a number of acute presentations of ischaemic heart disease.

It covers a number of presentations, including
- ST elevation myocardial infarction (STEMI)
- non-ST elevation myocardial infarction (NSTEMI)
- unstable angina

Unstable angina
- considered to be present in patients with ischaemic symptoms suggestive of an ACS and no elevation in troponins, with or without electrocardiogram changes indicative of ischaemia
- however, as a rise in troponins may take some hours it may be indistinguishable for NSTEMI initially and is therefore treated the same until the troponin result is known

Question 2

How does ACS develop?

Answer 2

ACS generally develops in patients who have ischaemic heart disease, either known or previously undetected. Ischaemic heart disease is a term synonymous with coronary heart disease and coronary artery disease. It describes the gradual build up of fatty plaques within the walls of the coronary arteries. This leads to two main problems:

1. Gradual narrowing, resulting in less blood and therefore oxygen reaching the myocardium at times of increased demand. This results in angina, i.e. chest pain due to insufficient oxygen reaching the myocardium during exertion
2. The risk of sudden plaque rupture. The fatty plaques which have built up in the endothelium may rupture leading to sudden occlusion of the artery. This can result in no blood/oxygen reaching the area of myocardium.

Question 3

Risk factors for ischaemic heart disease?

Answer 3

Question 4

Pathophysiology ischaemic heart disease?

Answer 4

Ischaemic heart disease is a complex process which develops over a number of years. A number of changes can be seen:
- initial endothelial dysfunction is triggered by a number of factors such as smoking, hypertension and hyperglycaemia
- this results in a number of changes to the endothelium including pro-inflammatory, pro-oxidant, proliferative and reduced nitric oxide bioavailability
- fatty infiltration of the subendothelial space by low-density lipoprotein (LDL) particles
- monocytes migrate from the blood and differentiate into macrophages. These macrophages then phagocytose oxidized LDL, slowly turning into large ‘foam cells’. As these macrophages die the result can further propagate the inflammatory process.
- smooth muscle proliferation and migration from the tunica media into the intima results in formation of a fibrous capsule covering the fatty plaque.

Question 5

Complications of atherosclerosis?

Answer 5

Once a plaque has formed a number of complications can develop:
- the plaque forms a physical blockage in the lumen of the coronary artery. This may cause reduced blood flow and hence oxygen to the myocardium, particularly at times of increased demand, resulting clinically in angina
- the plaque may rupture, potentially causing a complete occlusion of the coronary artery. This may result in a myocardial infarction

Question 6

Symptoms and signs of ACS?

Answer 6

The classic and most common feature of ACS is chest pain.
- typically central/left-sided
- may radiate to the jaw or the left arm
- often described as ‘heavy’ or constricting, ‘like an elephant on my chest’
- it should be noted however in real clinical practice patients present with a wide variety of types of chest pain and patients/doctors may confuse ischaemic pain for other causes such as dyspepsia
- certain patients e.g. diabetics/elderly may not experience any chest pain

Other symptoms in ACS include
- dyspnoea
- sweating
- nausea and vomiting

Patients presenting with ACS often have very few physical signs to ellicit:
- pulse, blood pressure, temperature and oxygen saturations are often normal or only mildly altered e.g. tachycardia
- if complications of the ACS have developed e.g. cardiac failure then clearly there may a number of findings
- the patient may appear pale and clammy

Question 7

Ix chest pain?

Answer 7

The two most important investigations when assessing a patient with chest pain are:
- ECG
- cardiac markers e.g. troponin

Question 8

Dx?

Answer 8

STEMI

RCA blockage - II, III, AVF

Question 9

Dx?

Answer 9

NSTEMI

On the ECG there is deep ST depression in I-III, aVF, and V3-V6. aVR also has ST elevation. Deep and widespread ST depression is associated with very high mortality because it signifies severe ischemia usually of LAD or left main stem.

Question 10

ECG changes + which coronary artery

Answer 10

Question 11

Management of ACS?

Answer 11

Once a diagnosis of ACS has been made there are a number of elements to treatment:
prevent worsening of presentation (i.e. further occlusion of coronary vessel)
revascularise (i.e. ‘unblock’) the vessel if occluded (patients presenting with a STEMI)
treat pain

A commonly taught mnemonic for the treatment of ACS is MONA:
Morphine
Oxygen
Nitrates
Aspirin

Whilst useful it should be remember that not all patients require oxygen therapy. British Thoracic Society guidelines are now widely adopted and oxygen should only be given if the oxygen saturations are < 94%.

For patients who’ve had a STEMI (i.e. one of the coronary arteries has become occluded) the priority of management is to reopen, or revascularise, the blocked vessel.
a second antiplatelet drug should be given in addition to aspirin.
- Options include clopidogrel, prasugrel and ticagrelor

for many years the treatment of choice was thrombolysis. This involved the intravenous administration of a thrombolytic or ‘clot-busting’ drug to breakdown the thrombus blocking the coronary artery
since the early 2000’s thrombolysis has been superseded by percutaneous coronary intervention (PCI). In this procedure the blocked arteries are opened up using a balloon (angioplasty) following which a stent may be deployed to prevent the artery occluding again in the future. This is done via a catheter inserted into either the radial or femoral artery

If a patient presents with an NSTEMI then a risk stratification tool (such as GRACE) is used to decide upon further management. If a patient is considered high-risk or is clinically unstable then coronary angiography will be performed during the admission. Lower risk patients may have a coronary angiogram at a later date.

Question 12

Secondary prevention ACS?

Answer 12

Patients who’ve had an ACS require lifelong drug therapy to help reduce the risk of a further event. Standard therapy comprises the following as a minimum:
- aspirin
- a second antiplatelet if appropriate (e.g. clopidogrel)
- a beta-blocker
- an ACE inhibitor
- a statin

Question 13

Clinical features ACS?

Answer 13

Features of acute coronary syndrome (ACS) include:
chest pain
- classically on the left side of the chest
- may radiate to the left arm or neck
- this may not always be present. Being elderly, diabetic or female makes an atypical presentation more likely
dyspnoea
nausea and vomiting
sweating
palpitations

Question 14

Management of ACS depends on?

Answer 14

The management of ACS depends on the particular subtype. NICE management guidance groups the patients into two groups:
1. STEMI
2. NSTEM/unstable angina

Question 15

Common management of all patients with ACS?

Answer 15

Initial drug therapy
aspirin 300mg
oxygen should only be given if the patient has oxygen saturations < 94% in keeping with British Thoracic Society oxygen therapy guidelines
morphine should only be given for patients with severe pain
- previously IV morphine was given routinely
- evidence, however, suggests that this may be associated with adverse outcomes
nitrates
- can be given either sublingually or intravenously
- useful if the patient has ongoing chest pain or hypertension
- should be used in caution if patient hypotensive

The next step in managing a patient with suspected ACS is to determine whether they meet the ECG criteria for STEMI.

STEMI criteria
clinical symptoms consistent with ACS (generally of ≥ 20 minutes duration) with persistent (> 20 minutes) ECG features in ≥ 2 contiguous leads of:
- 2.5 mm (i.e ≥ 2.5 small squares) ST elevation in leads V2-3 in men under 40 years, or ≥ 2.0 mm (i.e ≥ 2 small squares) ST elevation in leads V2-3 in men over 40 years
- 1.5 mm ST elevation in V2-3 in women
- 1 mm ST elevation in other leads
- new LBBB (LBBB should be considered new unless there is evidence otherwise)

Question 16

STEMI criteria?

Answer 16

STEMI criteria
clinical symptoms consistent with ACS (generally of ≥ 20 minutes duration) with persistent (> 20 minutes) ECG features in ≥ 2 contiguous leads of:
- 2.5 mm (i.e ≥ 2.5 small squares) ST elevation in leads V2-3 in men under 40 years, or ≥ 2.0 mm (i.e ≥ 2 small squares) ST elevation in leads V2-3 in men over 40 years
- 1.5 mm ST elevation in V2-3 in women
- 1 mm ST elevation in other leads
- new LBBB (LBBB should be considered new unless there is evidence otherwise)

Question 17

Management of STEMI?

Question 18

First step after confirming STEMI?

Answer 18

Once a STEMI has been confirmed the first step is to immediately assess eligibility for coronary reperfusion therapy. There are two types of coronary reperfusion therapy:
percutaneous coronary intervention
- should be offered if the presentation is within 12 hours of the onset of symptoms AND PCI can be delivered within 120 minutes of the time when fibrinolysis could have been given (i.e. consider fibrinolysis if there is a significant delay in being able to provide PCI)
- If patients present after 12 hours and still have evidence of ongoing ischaemia then PCI should still be considered
- drug-eluting stents are now used. Previously ‘bare-metal’ stents were sometimes used but have higher rates of restenosis
- radial access is preferred to femoral access

fibrinolysis
- should be offered within 12 hours of the onset of symptoms if primary PCI cannot be delivered within 120 minutes of the time when fibrinolysis could have been given
- a practical example may be a patient who presents with a STEMI to a small district general hospital (DGH) that does not have facilities for PCI. If they cannot be transferred to a larger hospital for PCI within 120 minutes then fibrinolysis should be given. If the patient’s ECG taken 90 minutes after fibrinolysis failed to show resolution of the ST elevation then they would then require transfer for PCI

Question 19

Drugs to be taken before + during PCI?

Answer 19

Further antiplatelet prior to PCI
this is termed ‘dual antiplatelet therapy’, i.e. aspirin + another drug
if the patient is not taking an oral anticoagulant: prasugrel
if taking an oral anticoagulant: clopidogrel

Drug therapy during PCI
patients undergoing PCI with radial access:
- unfractionated heparin with bailout glycoprotein IIb/IIIa inhibitor (GPI) - this is the action of using a GPI during the procedure when it was not intended from the outset, e.g. because of worsening or persistent thrombus
patients undergoing PCI with femoral access:
- bivalirudin with bailout GPI

Question 20

Once fibrinolysis commenced what should be done?

Answer 20

Patients undergoing fibrinolysis should also be given an antithrombin drug.

An ECG should be repeated after 60-90 minutes to see if the ECG changes have resolved. If patients have persistent myocardial ischaemia following fibrinolysis then PCI should be considered.

Question 21

Management of NSTEMI/unstable angina?

Answer 21

Question 22

What is antithrombin treatment?

Answer 22

(in tx of NSTEMI)

antithrombin treatment
- fondaparinux should be offered to patients who are not at a high risk of bleeding and who are not having angiography immediately
- if immediate angiography is planned or a patients creatinine is > 265 µmol/L then unfractionated heparin should be given

Question 23

GRACE tool?

Answer 23

The Global Registry of Acute Coronary Events (GRACE) is the most widely used tool for risk assessment. It can be calculated using online tools and takes into account the following factors:
age
heart rate, blood pressure
cardiac (Killip class) and renal function (serum creatinine)
cardiac arrest on presentation
ECG findings
troponin levels

This results in the patient being risk stratified as follows:

Question 24

Which patients with NSTEMI/unstable angina should have coronary angiography +/- PCI?

Answer 24

immediate: patient who are clinically unstable (e.g. hypotensive)

within 72 hours: patients with a GRACE score > 3% i.e. those at intermediate, high or highest risk

coronary angiography should also be considered for patients if ischaemia is subsequently experienced after admission

Question 25

Further drug therapy for patients with NSTEMI/unstable angina following PCI?

Answer 25

Further drug therapy

unfractionated heparin should be given regardless of whether the patient has had fondaparinux or not

further antiplatelet (‘dual antiplatelet therapy’, i.e. aspirin + another drug) prior to PCI
- if the patient is not taking an oral anticoagulant: prasugrel or ticagrelor
- if taking an oral anticoagulant: clopidogrel

Question 26

Conservative management for patients with NSTEMI/unstable angina?

Answer 26

further antiplatelet (‘dual antiplatelet therapy’, i.e. aspirin + another drug)
- if the patient is not at a high risk of bleeding: ticagrelor
- if the patient is at a high risk of bleeding: clopidogrel

Question 27

Prognosis ACS?

Answer 27

*Killip class - system used to stratify risk post myocardial infarction